Abstract
The present experiment was undertaken to elucidate the simultaneous effect of clonidine on ambulatory activity and water drinking behavior in spontaneously hypertensive rats (SHR). An attempt was also made to determine the role of sympathetic nerve activity in the mechanism of clonidine-induced sedation in SHR. The sensitive method developed by Tadokoro et al. for simultaneous determination of ambulatory activity and drinking behavio in rats was used. Clonidine (150μ Eg/kg, po twice daily) produced a significant decrease in ambulatory activity and water drinking behavior at the beginning of the dark phase in twenty week old male SHR of Wistar Okamoto strain. Clonidine produced an increase in water drinking behavior in the light phase which was not observed in the control period. Under the same experimental conditions, the lowering of brain stem norepinephrine content produced by diethyl dithiocarbamate appeared to be inhibited in clonidine-treated SHR in the dark phase. Clonidine significantly decreased urinary norepinephrine content in the dark phase. On the other hand, clonidine (30μ g/kg, iv) produced a decrease in efferent nerve discharges of splanchnic nerve and sympathetic adrenal nerve in SHR. These findings suggest that decreased sympathetic nerve activity via a centrally mediated mechanism is at least in part associated with the decreased ambulatory activity induced by clonidine.
